Gastrin-stimulated changes in Ca2+ concentration in parietal cells depends on adenosine 3',5'-cyclic monophosphate levels.

Abstract

The parietal cell has secretory receptors for histamine and acetylcholine, whereas the functional nature of the gastrin/cholecystokinin B receptor is controversial. This study in isolated gastric glands investigates the cholecystokinin B receptor-induced intracellular calcium concentration ([Ca]i) response in enterochromaffin-like (ECL) and parietal cells as a function of adenosine 3',5'-cyclic monophosphate pathways. The responses of [Ca]i in ECL and parietal cells of perfused rabbit or rat calcium orange-loaded gastric glands were determined using confocal microscopy. ECL cells were identified by position, size, and autofluorescence and parietal cells by position and size. Gastrin (1 mumol/L) produced an elevation of [Ca]i levels in both ECL and parietal cells. In the presence of 100 mumol/L cimetidine, the ECL cell response to gastrin was not affected but the [Ca]i response of the parietal cell was abolished. With dibutyryl adenosine 3',5' phosphate in addition to cimetidine, the response of the parietal cell [Ca]i to gastrin was restored in both the rat and rabbit. The [Ca]i response of the parietal but not the ECL cell to the addition of gastrin seems to depend on the presence of normal or elevated intracellular adenosine 3',5'-cyclic monophosphate levels. Therefore, H2 receptor activity may be permissive for the effect of gastrin on parietal cell function.